Changes in Radial Artery Pulse Pressure During a Fluid Challenge Cannot Assess Fluid Responsiveness in Patients With Septic Shock

2017 ◽  
Vol 35 (2) ◽  
pp. 149-153
Author(s):  
Victor De la Puente-Diaz de Leon ◽  
Valente de Jesus Jaramillo-Rocha ◽  
Jean-Louis Teboul ◽  
Sofia Garcia-Miranda ◽  
Bernardo A. Martinez-Guerra ◽  
...  

Background: Arterial blood pressure is the most common variable used to assess the response to a fluid challenge in routine clinical practice. The aim of this study was to evaluate the accuracy of the change in the radial artery pulse pressure (rPP) to detect the change in cardiac output after a fluid challenge in patients with septic shock. Methods: Prospective observational study including 35 patients with septic shock in which rPP and cardiac output were measured before and after a fluid challenge with 400 mL of crystalloid solution. Cardiac output was measured with intermittent thermodilution technique using a pulmonary artery catheter. Patients were divided between responders (increase >15% of cardiac output after fluid challenge) and nonresponders. The area under the receiver operating characteristic curve (AUROC), Pearson correlation coefficient and paired Student t test were used in statistical analysis. Results: Forty-three percent of the patients were fluid responders. The change in rPP could not neither discriminate between responders and nonresponders (AUROC = 0.52; [95% confidence interval: 0.31-0.72] P = .8) nor correlate ( r = .21, P = .1) with the change in cardiac output after the fluid challenge. Conclusions: The change in rPP neither discriminated between fluid responders and nonresponders nor correlated with the change in cardiac output after a fluid challenge. The change in rPP cannot serve as a surrogate of the change in cardiac output to assess the response to a fluid challenge in patients with septic shock.

Author(s):  
Fiona Roberts ◽  
Alan Gaffney

This chapter discusses vasodilatory shock. The hallmark of vasodilatory shock is hypotension with normal or increased cardiac output. The hyperdynamic circulatory state of vasodilatory shock results in a tachycardia and an increased pulse pressure. Radiological and biochemical investigations can assist with determining the diagnosis of shock. The causes of vasodilatory shock are diverse; they include sepsis, surgical insult, anaphylaxis, and others such as trauma, burns, and pancreatitis. However, sepsis is by far the most common cause of vasodilatory shock. The pathophysiology of vasodilatory shock is also complex and multifactorial. Although still not fully understood, it is widely accepted that it includes activation of several intrinsic vasodilatory pathways and a vascular hyporesponsiveness to vasopressors. Early fluid resuscitation and appropriate antimicrobial therapy are the most crucial treatment interventions in septic shock. Meanwhile, noradrenaline is the first-line vasopressor of choice in septic shock.


1965 ◽  
Vol 20 (1) ◽  
pp. 137-141 ◽  
Author(s):  
Gunnar Grimby

Clearance of inulin (CIn) and para-aminohippuric acid (CPAH), cardiac output, oxygen uptake, and arterial blood pressure were measured in five healthy subjects at rest and during supine exercise on a bicycle ergometer before and after injection of a bacterial pyrogen (purified lipopolysaccharide, Pyrexal). CPAH was 45–145% higher at rest during the flush phase than in the normal condition. The increase in CIn, was less. Cardiac output increased also. The renal fraction of the cardiac output was larger than in the normal condition. During moderate exercise in the flush phase, CPAH decreased from the values before work. This decrease was usually larger than in the normal condition. The pyrogen-induced increase in cardiac output was less during exercise than at rest. A pronounced renal vasoconstriction during exercise is demonstrated even after the injection of bacterial pyrogen. clearance of inulin and para-aminohippuric acid; cardiac output; extraction ratio Submitted on May 4, 1964


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Zakaria Ait-Hamou ◽  
Jean-Louis Teboul ◽  
Nadia Anguel ◽  
Xavier Monnet

Abstract Background Volume expansion is aimed at increasing cardiac output (CO), but this variable is not always directly measured. We assessed the ability of changes in arterial pressure, pulse pressure variation (PPV) and heart rate (HR) or of a combination of them to detect a positive response of cardiac output (CO) to fluid administration. Methods We retrospectively included 491 patients with circulatory failure. Before and after a 500-mL normal saline infusion, we measured CO (PiCCO device), HR, systolic (SAP), diastolic (DAP), mean (MAP) and pulse (PP) arterial pressure, PPV, shock index (HR/SAP) and the PP/HR ratio. Results The fluid-induced changes in HR were not correlated with the fluid-induced changes in CO. The area under the receiver operating characteristic curve (AUROC) for changes in HR as detectors of a positive fluid response (CO increase ≥ 15%) was not different from 0.5. The fluid-induced changes in SAP, MAP, PP, PPV, shock index (HR/SAP) and the PP/HR ratio were correlated with the fluid-induced changes in CO, but with r < 0.4. The best detection was provided by increases in PP, but it was rough (AUROC = 0.719 ± 0.023, best threshold: increase ≥ 10%, sensitivity = 72 [66–77]%, specificity = 64 [57–70]%). Neither the decrease in shock index nor the changes in other indices combining changes in HR, shock index, PPV and PP provided a better detection of a positive fluid response than changes in PP. Conclusion A positive response to fluid was roughly detected by changes in PP and not detected by changes in HR. Changes in combined indices including the shock index and the PP/HR ratio did not provide a better diagnostic accuracy.


1981 ◽  
Vol 240 (3) ◽  
pp. H421-H429 ◽  
Author(s):  
G. Baccelli ◽  
R. Albertini ◽  
A. Del Bo ◽  
G. Mancia ◽  
A. Zanchetti

To evaluate whether sinoaortic afferents contribute to the hemodynamic pattern of fighting, cardiovascular changes associated with fighting were studied in cats before and after sinoaortic denervation. Sinoaortic denervation exaggerates the decrease in heart rate, cardiac output, and arterial pressure during immobile confrontation (hissing, staring but no movement). During nonsupportive fighting (fighting with forelimbs while lying on one side) and supportive fighting ( fighting while standing on four feet) sinoaortic denervation reduces the increase in heart rate and cardiac output, minimizes the mesenteric vasoconstriction, induces a fall in arterial blood pressure, but does not affect iliac vasoconstriction or vasodilatation. The hemodynamic pattern of fighting is similarly changed by temporary inactivation of carotid sinus baroreflexes by common carotid occlusion as by chronic section of sinoaortic nerves. It is concluded that sinoaortic reflexes play an important role in the cardiovascular patterns accompanying natural fighting. They favor cardiac action and allow a marked visceral vasoconstriction to occur, thus minimizing or preventing a fall in blood pressure during emotional behavior.


1963 ◽  
Vol 41 (11) ◽  
pp. 2337-2341 ◽  
Author(s):  
Elwood W. Speckmann ◽  
Robert K. Ringer

The cardiac output of untreated mature male Broad Breasted Bronze (BBB) turkeys was determined by an isotope dilution technique using radioactive phosphorus (P32). A Geiger–Mueller tube was connected to a rate meter which in turn was connected to a moving graph to continuously record the indicator concentration, thus obtaining the initial dilution curve. Posterior tibial and common carotid arterial blood pressures were measured directly and were recorded simultaneously with the cardiac output determinations by means of two strain gauges connected to a recording polygraph.From the cardiovascular measurements systemic resistance was calculated. The mean cardiac output of the mature male BBB turkey was 231 ml per kg body weight0.734 per minute. The mean carotid hemodynamic parameters were: systolic BP, 302 mm Hg; diastolic BP, 204 mm Hg; and pulse pressure, 98 mm Hg. Heart rate was 149 beats per minute. The mean tibial hemodynamic parameters were; systolic BP, 286 mm Hg; diastolic BP, 200 mm Hg; and pulse pressure, 85 mm Hg. The mean systemic resistance units were 0.17 and 0.16 for carotid and tibial arteries respectively on a bird basis and 1.13 and 1.08 respectively per kg body weight0.734.


2004 ◽  
Vol 106 (4) ◽  
pp. 365-369 ◽  
Author(s):  
Marcel AZABJI KENFACK ◽  
Federic LADOR ◽  
Marc LICKER ◽  
Christian MOIA ◽  
Enrico TAM ◽  
...  

Modelflow®, when applied to non-invasive fingertip pulse pressure recordings, is a poor predictor of cardiac output (Q, litre·min-1). The use of constants established from the aortic elastic characteristics, which differ from those of finger arteries, may introduce signal distortions, leading to errors in computing Q. We therefore hypothesized that peripheral recording of pulse pressure profiles undermines the measurement of Q with Modelflow®, so we compared Modelflow® beat-by-beat Q values obtained simultaneously non-invasively from the finger and invasively from the radial artery at rest and during exercise. Seven subjects (age, 24.0±2.9 years; weight, 81.2±12.6 kg) rested, then exercised at 50 and 100 W, carrying a catheter with a pressure head in the left radial artery and the photoplethysmographic cuff of a finger pressure device on the third and fourth fingers of the contralateral hand. Pulse pressure from both devices was recorded simultaneously and stored on a PC for subsequent Q computation. The mean values of systolic, diastolic and mean arterial pressure at rest and exercise steady state were significantly (P<0.05) lower from the finger than the intra-arterial catheter. The corresponding mean steady-state Q obtained from the finger (Qporta) was significantly (P<0.05) higher than that computed from the intra-arterial recordings (Qpia). The line relating beat-by-beat Qporta and Qpia was y=1.55x-3.02 (r2=0.640). The bias was 1.44 litre·min-1 and the precision was 2.84 litre·min-1. The slope of this line was significantly higher than 1, implying a systematic overestimate of Q by Qporta with respect to Qpia. Consistent with the tested hypothesis, these results demonstrate that pulse pressure profiles from the finger provide inaccurate absolute Q values with respect to the radial artery, and therefore cannot be used without correction with a calibration factor calculated previously by measuring Q with an independent method.


1963 ◽  
Vol 41 (1) ◽  
pp. 2337-2341 ◽  
Author(s):  
Elwood W. Speckmann ◽  
Robert K. Ringer

The cardiac output of untreated mature male Broad Breasted Bronze (BBB) turkeys was determined by an isotope dilution technique using radioactive phosphorus (P32). A Geiger–Mueller tube was connected to a rate meter which in turn was connected to a moving graph to continuously record the indicator concentration, thus obtaining the initial dilution curve. Posterior tibial and common carotid arterial blood pressures were measured directly and were recorded simultaneously with the cardiac output determinations by means of two strain gauges connected to a recording polygraph.From the cardiovascular measurements systemic resistance was calculated. The mean cardiac output of the mature male BBB turkey was 231 ml per kg body weight0.734 per minute. The mean carotid hemodynamic parameters were: systolic BP, 302 mm Hg; diastolic BP, 204 mm Hg; and pulse pressure, 98 mm Hg. Heart rate was 149 beats per minute. The mean tibial hemodynamic parameters were; systolic BP, 286 mm Hg; diastolic BP, 200 mm Hg; and pulse pressure, 85 mm Hg. The mean systemic resistance units were 0.17 and 0.16 for carotid and tibial arteries respectively on a bird basis and 1.13 and 1.08 respectively per kg body weight0.734.


Author(s):  
Arthur Le Gall ◽  
Fabrice Vallée ◽  
Jona Joachim ◽  
Alex Hong ◽  
Joaquim Matéo ◽  
...  

AbstractMulti-beat analysis (MBA) of the radial arterial pressure (AP) waveform is a new method that may improve cardiac output (CO) estimation via modelling of the confounding arterial wave reflection. We evaluated the precision and accuracy using the trending ability of the MBA method to estimate absolute CO and variations (ΔCO) during hemodynamic challenges. We reviewed the hemodynamic challenges (fluid challenge or vasopressors) performed when intra-operative hypotension occurred during non-cardiac surgery. The CO was calculated offline using transesophageal Doppler (TED) waveform (COTED) or via application of the MBA algorithm onto the AP waveform (COMBA) before and after hemodynamic challenges. We evaluated the precision and the accuracy according to the Bland & Altman method. We also assessed the trending ability of the MBA by evaluating the percentage of concordance with 15% exclusion zone between ΔCOMBA and ΔCOTED. A non-inferiority margin was set at 87.5%. Among the 58 patients included, 23 (40%) received at least 1 fluid challenge, and 46 (81%) received at least 1 bolus of vasopressors. Before treatment, the COTED was 5.3 (IQR [4.1–8.1]) l min−1, and the COMBA was 4.1 (IQR [3–5.4]) l min−1. The agreement between COTED and COMBA was poor with a 70% percentage error. The bias and lower and upper limits of agreement between COTED and COMBA were 0.9 (CI95 = 0.82 to 1.07) l min−1, −2.8 (CI95 = −2.71 to−2.96) l min−1 and 4.7 (CI95 = 4.61 to 4.86) l min−1, respectively. After hemodynamic challenge, the percentage of concordance (PC) with 15% exclusion zone for ΔCO was 93 (CI97.5 = 90 to 97)%. In this retrospective offline analysis, the accuracy, limits of agreements and percentage error between TED and MBA for the absolute estimation of CO were poor, but the MBA could adequately track induced CO variations measured by TED. The MBA needs further evaluation in prospective studies to confirm those results in clinical practice conditions.


1982 ◽  
Vol 52 (1) ◽  
pp. 206-215 ◽  
Author(s):  
R. S. Lillo ◽  
D. R. Jones

Control of hyperpnea during recovery from diving in unanesthetized White Pekin ducks, Anas platyrhynchos, was examined. Postdive minute ventilation (VE) increased five times regardless of the length of the preceding dive (1–4 min), although longer dives resulted in slower return of VE towards predive levels. Manipulation of arterial blood gases showed that both hypoxia and hypercapnia contributed to hyperpnea on emergence. Although chronic bilateral carotid body denervation depressed VE before and after diving, VE still increased four times after 1-min dives. Postdive hyperpnea was accompanied by dramatic elevations in heart rate, cardiac output, and the ventilation/perfusion ratio. However, artificially maintaining heart rate at abnormally low levels did not affect the postdive hyperpnea. In addition, postdive hyperpnea was unaffected by systemic arterial baroreceptor denervation. Postdive hyperpnea in ducks depends on blood gas changes occurring during a dive, yet a substantial part of the response is independent of input from carotid body chemoreceptors and the accompanying rises in heart rate and cardiac output.


1962 ◽  
Vol 39 (2) ◽  
pp. 308-322 ◽  
Author(s):  
Göran Bojs ◽  
Thomas Falkheden ◽  
Björn Sjögren ◽  
Edvardas Varnauskas

ABSTRACT Determinations of cardiac output and oxygen consumption simultaneously with measurements of glomerular filtration rate and renal plasma flow were performed before and after hypophysectomy in two cases of acromegaly, two cases of metastatic mammary carcinoma, one case of diabetes mellitus and in one case of chromophobe adenoma. After hypophysectomy evidence of adrenocortical insufficiency was present in all but one subject and these patients were on substitution therapy with cortisone (17,21-dihydroxy-pregn-4-ene 3,11,20-trione) at the time of the postoperative studies. In two patients at least, postoperative hypothyroidism could not be demonstrated. In all cases, however, hypophysectomy was followed by a marked and roughly parallel reduction in cardiac output and oxygen consumption. A substantial decrease in glomerular filtration rate, renal plasma flow and renal blood flow following hypophysectomy was also found while no or only slight changes in mean brachial arterial blood pressure were observed. The changes in renal function did not always parallel the reduction in cardiac output.


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